Cardac Arrhythmia Drugs Flashcards
(53 cards)
What are arrhythmia
Heart condition where disturbances in – Pacemaker impulse formation – Contraction impulse conduction – Combination of the two Results in rate and/or timing of contraction of heart muscle that may be insufficient to maintain normal cardiac output (CO)
Describe thr eating potential
• A transmembrane electrical gradient (potential) is maintained, with the interior of the cell negative with respect to outside the cell
• Caused by unequal distribution of ions inside vs. outside cell
– Na+ higher outside than inside cell
– Ca+ much higher outside than inside cell – K+ higher inside cell than outside
• Maintenance by ion selective channels, active pumps and exchangers
Desribe the fats cardiac AP
Ss
Describe how class 1 drugs work
Block Na+ channels — Marked slowing conduction in tissue (phase 0) Minor effects on action potential duration (APD)
Describe how class 2 drugs work
Beta blockers — Diminish phase 4 depolarisation and automaticity
Slightly increasing refractory period. Affects depolarisation
Desribe how class 3 drugs work
Block k channels
Increase action potential duration (APD) (plateau phase increased)
Risky - can overlap with other beats - pro arrhythmic?
Describe how class 4 drugs work
Ccb Calcium channel blockers decrease inward Ca2+ currents resulting in a decrease of phase 4 spontaneous depolarization
Effect plateau phase of action potential
Reduced plateau, effect on phase 4 depolarisation
Describe the slow cardiac ap
Ss
Describ ethe efect of Ca2+ blockers on the slow cap
Slope of phase 0 = Conduction velocity
Reduces slope
Describe drugs affecting automaticity
Change phase 4 - beta blockers may be effective at reducing these affects
Muscarinic agonists, Adenosine
???
Gove an overview of mechanisms of arrythmogenesis
Abnormal impulse generation
- Automatic rhytms
- Triggered rhythms
Abnormal conduction
- COnduction block
- Re-entry
How can absonral conduction occur
Ss
Drive abnormal atomic conduction
Present only in small populations
•Lead to preexcitation→Wolf-Parkinson-White Syndrome (WPW)
Ss
Describe re-entry
S
Describe the actio of drugs to treat abnormal generation
Descrease of phase 4 slope in pacemaker cells - slow the automaticity
Raise the threshold - in order to generate impulse, have to have AP above a certain point
Describe the actio of drugs in the case of abnormal condition
Decrease conduction velocity
Increase ERP so ckd cant be reexcited agai
Descrive pharmacologic rationale ad goals
• Goal:
- restore normal sinus rhythm and conduction
- prevent more serious and possibly lethal arrhythmias from occurring
• Antiarrhythmic drugs are used to:
- decrease conduction velocity
- change the duration of ERP
- suppress abnormal automaticity
Give an overview of the drugs used
Ss
Descrive class 1a agents
Class 1A agents: Procainamide, quinidine, disopyramide
Absorption and elimination (oral or iv)
What are the effects of 1A on cardiac activity
Effects on cardiac activity
^ conduction (v phase 0 of the action potential (Na+))
^ refractory period (^APD (K+) and^Na inactivation)
V automaticity (v slope of phase 4, fast potentials)
^increase threshold (Na+)
Quinidine has anticholinergic (atropine like action) to speed AV conduction used with digitalis, β blocker or Ca channel blocker
Effects on ECG ^ QRS, +/- PR, ^QT
Wat are the uses of 1A
Wide spectrum:
Quinidine : maintain sinus rhythms in atrial fibrillation and flutter
and to prevent recurrence, Brugada syndrome
Procainamide: acute IV treatment of supraventricular and
ventricular arrhythmias
What are the side effects of 1A drugs
Hypotension, reduced cardiac output
Proarrhythmia (generation of a new arrhythmia) - eg.Torsades de Points (increased QT interval)
Dizziness, confusion, insomnia, seizure (high dose)
Gastrointestinal effects (common)
Lupus-like syndrome (esp. procainamide)
What are class 1B
Class 1B agents: Lidocaine, mexiletine
Absorption and elimination
Lidocaine: iv only (initially)
Mexiletine: oral (long term)
What are the effects of class 1B drugs on cardiac activity and ECG
Effects on cardiac activity
Fast binding offset kinetics
No change in phase 0 in normal tissue (no tonic block)
APD slightly decreased (normal tissue)
Increase threshold (Na+)
Decrease phase 0 conduction in fast beating or ischaemic tissue,
Effects on ECG
None in normal, in fast beating or ischaemic increase QRS
